Psychiatry & Psychotherapy Podcast - COVID-19 and the Brain: Delirium & Viral Encephalitis

Episode Date: April 4, 2020

In a previous episode, we covered COVID-19 and its effect on mental health. In today's episode of the podcast, we will be covering COVID-19 from the medical perspective with regards to its effect on the brain as well as treatment options, their side effects and special considerations. By listening to this episode, you can earn 0.75 Psychiatry CME Credits. Link to blog. Link to YouTube video.

Hello and welcome to the Psychiatry and Psychotherapy Podcast. I'm here to talk about getting rid of burnout, increasing job satisfaction, and feeling like an expert in what you do. One thing that created a lot of burnout and angst for me was trying to get continued medical education right at the last minute. So why not join the CME membership and do CMEE while listening to this podcast? Go to Psychiatrypodcast.com, sign up, sign in, take the test, and the certification is email to you in seconds.

Hello and welcome back to the podcast. Today, I am going to be doing a dive into some of the neurologic and psychiatric complications of COVID-19. It's a little bit more of a sobering podcast. And in this time, I'm reminded of one of my favorite books, Man's Search for Meeting, Victor Frankel. He wrote about the intimate and horrific Holocaust experience that he viewed from the perspective of a psychiatrist.

And he said, the way in which a man accepts his fate and all the suffering entails, the way in which he takes up his cross gives him ample opportunity, even under the most difficult circumstances, to add a deeper meaning to his life. It may remain brave, dignified, and unselfish, or in the bitter fight for self-preservation,

he may forget his human dignity and become no more than an animal. He also was quoted to say, We who lived in the concentration camps can remember the men who walked through the huts, comforting others, last piece of bread. They may have been few in number, but they offer sufficient proof that everything can be taken away from a man, but one thing, the last of human freedoms, to choose

one's attitude in any given set of circumstances, to choose one's own way. So as I think about this time that we're in, this unique time, this time of coming together, of bonding together, of overcoming together, striving to overcome together. It's like a war time. It's like a war time. of sorts in the medical field. People are dying. Just this last week, two residents died in New York. You know, these are people who are at the beginning of their career. It's tragic. Likely more will come. And this episode is really more about the science. So if you're a psychiatrist, if you're treating people on the front lines of this, this might be a good episode to kind of talk about some of the nuances of delirium, the nuances of encephalopathy, and how common things like stroke and

delirium are in this population. I'm also going to talk about the neuroinvasive potential of this disease COVID-19 and how it's been shown to travel through the nose to the brain and how an osmia, a loss of smell is actually very, very common, maybe even before some of the other symptoms are present. So this is kind of a psychiatrist's perspective of COVID-19 and the treatment of it. I got an undergrad degree from UC Berkeley in molecular and cell biology, an emphasis in immunology,

and then went to medical school, went to psychiatry residency, and work largely in an IOP and partial consult and liaison type psychiatry setting. And I do cover the CNL unit for my university, Lomeland University, when Dr. Lee, who's our main CNL guy, is gone. So that's my credentials to talk about this. And for the last couple weeks, I've been in the midst of this, right? All of us as physicians are literally being updated. every day and on new protocols and new sort of ways of approaching this.

So I decided to utilize my team of medical students and my own digging to come up with kind of a detailed report. It'll be on my website. Along with what I'm going to present today, I do this a little bit with some realism of the gravity of the situation that we have, but also with the desire not to increase anxiety, but hopefully decrease anxiety as we become more nuanced in our treatment and knowledge of this. So here we go. In December 2019, a virus coined 2019 novel coronavirus was isolated from patients. with pneumonia of an unknown ideology in Wuhan, China.

The 2019 novel coronavirus was soon renamed Coronavirus Disease COVID-19 by the World Health Organization on February 11, 2020, and severe acute respiratory syndrome coronavirus to SARS-CoV-2 by the International Committee of Taxonomy, of viruses, just to give some background information before I jump into the psychiatric manifestations and such. This virus has been linked to a seafood market, a large live animal in seafood market that sold exotic animals, including bats. And through genomic testing, the SARS-CoV-2

was shown to be a positive strand, single-stranded RNA virus, closely related. to the bat-derived SARS-like coronavirus. Based on the genomic evidence and the fact that most of the infected patients recently visit the Hunan seafood market, the SARS-CoV-2, most likely mutated from a bat virus and was introduced through live bats or animal products contaminated with bat droppings. So on January 30th, 2020, the WHO declared the COVID-19 a public health emergency of international concern.

The other five times this has happened was the Keevi Ebola in the Democratic Republic of Congo in 2019, the Zika virus in 2016, the Ebola virus in West Africa in 2014, polio in 2014, and the H1N1 in 2009. A little bit on the epidemiology.

As of April 2nd, 2020, who reports that there have been 896,000 confirmed cases of COVID-19 globally and 72,000 new cases in the last 24 hours. 45,000 deaths thus far and 4,924 deaths in the past 24 hours. It's coming from the WHO website at the time of the recording of this podcast, which is on April 4th. in the U.S. there have been 140,000 confirmed cases and 17,000, almost 18,000 in the last 24 hours. There have been 2,300 deaths thus far. Contributing factors to the rapid spread of COVID-19 worldwide include the mode of transmission,

transmission through asymptomatic carriers, and the ease and convenience of global travel, multiple studies have shown that transmission of the SARS-CoV-2 in-person-to-person through droplets of cough and sneeze and direct contact, breathing, as well as fomites. Recent study, Van Dormelan, 2020, tested the susceptibility and viability of the SARS-CoV-2 on five environmental places. they found that the virus can live in the air for about three hours as droplets and could survive for about four hours on copper of up to 24 hours on cardboard and up to three days on steel and plastic. If you read the paper in particular, it was more talking about the rate of decrease. And so these details are likely to change.

and be different in different circumstances, I imagine. Our current understanding is that the mean incubation period is five to six days. This number has moved around a little bit, but the CDC, the WHO, and the European Center of Disease Prevention and Control all say that the incubation period can be one to 14 days, which is why this is such a virulent or easily spread illness because so many people are spreading it without even knowing that they're sick. All of these factors in conjunction with a high possibility of transmission through asymptomatic carriers and global travel have resulted in the explosive rise of cases, which are likely going to continue to increase. We'll talk a little bit about the clinical manifestations and then we'll go more into the. the neurological manifestations.

So the most common symptoms are fever, followed by cough, upper respiratory congestion, dysknea, myalgas, fatigue, and headache. Less common are hemoptosis and diarrhea. Among patients with dyspnea, many need intensive care with ventilation, and this is becoming quite the problem as ventilators are limited. When I was watching news recently, I felt very sentimental when I was hearing about how machines that are being used for surgery are potentially going to be used. And there definitely is a rallying around trying to get more machines for patients. But this has been an issue in places like Italy and New York.

So complications due to COVID-19 include ARDS, ARDS, ARDS, and with these classic ground glass of papyrs, is noted on chest imaging. Patients can also have acute cardiac injury with elevated troponins and secondary infection. So infection with like bacteria or other viruses. Risk factors increased morbidity and mortality associated with COVID-19 included include older age and a comorbid health complication

such as diabetes, hypertension, shribovascular disease, cardiovascular disease and delirium. Recently there has been new evidence for anosmia, loss of smell, in patients with COVID-19, and maybe even early on patients may have this. In the United Kingdom, they discussed this in a paper that summarized the report from Germany that two out of three confirmed cases of COVID-19 had this loss of smell. and in South Korea, where they did a lot more testing, 30% of patients with mild symptoms

tested positive for COVID-19. So in this article that I was reading, they recommended an osmia being added to COVID-19 symptoms and used for potential screening. Okay, now to get into some of the things from a psychiatric and neurological perspective, Although pulmonary like ARDS and cardiac complications like acute cardiac injury have been a large focus of the medical complications in the COVID-19 recent literature, neurological like delirium and cerebrovascular like stroke events associated with COVID-19 have recently been something of increased focus and concentration. previous studies on the coronavirus such as the SARS-CoV-1 and the MERS cove had neuroinvasive potential and seemed to favor the brain stem specifically in where they would be infecting. Additionally, these same studies have shown that the coronavirus may initially invade peripheral nerve terminals

and through trans-synaptic transfer gain access to the CNS, the central nervous system. So there's a possibility that it's traveling through the nerves to the brain. Many institutions are reporting an increased incidence of anosmia, a loss of smell in patients who tested positive for this virus. A cross-sectional study in Iran showed a significant correlation between endosmia and COVID-19 patients. the correlation was 0.87, so it's pretty high correlation. The onset of anosmia was sudden in 76% of patients and 60% had continued decreased sense of smell. Like I said before earlier, other countries in Germany

and Korea have also reported high findings of that symptom. loss of smell. So could there be a tie between this loss of smell and the profound dyspnea, the shortness of breath and severe cases? A study in the Journal of Medical Virology in 2020 by Lee et al described how the nose is directly linked to the brain and further increased incidence shows that coronaviruses may first invade peripheral nerve terminals, especially the olifactyl. nerve and proceeding to gain access to the CNS through this sort of synapse-connected route. The sister SARS-Cove virus has been studied much more in depth because it was, you know, been around longer, and it showed that there was virus in the brain in both patients and animals,

experimental animals, where the brain stem was heavily infected. For instance, experimental studies using transgenic mice reveal that SARS-CoV, when given intranasally, could enter the brain possibly via the olfactory nerves and thereby rapidly spread to specific areas of the brain, including the thalamus of the brainstem. It is quite likely that potential neuroinvation of the SARS-CoV-2 is at least partially responsible for the acute respiratory failure of the COVID-19 patients. if neuroinvasion of the SARS-CoV-2 does take place in the development of respiratory failure, the precaution with masks, the precaution for using masks,

will absolutely be the most effective measure to protect against the entry of the virus into the CNS. In addition to this loss of smell numerous, other neurological symptoms have been reported worldwide, a retrospective case series in three designated COVID-19 care hospitals of the Union Hospital of Hous Hong, University of Science Technology, and Wuhan, China reported three main areas of concern. They found, and this was an article in 2020, Mao at all, that the central nervous system, most commonly had complaints of dizziness, 16% of patients, headaches and 13%. And they also found that the rates of acute cerebrovascular disease, so basically stroke, was 5.7% in the severely ill and 0.8% in the less severely ill COVID-19 patients.

They found that impaired consciousness was found in 14.8% of the severely ill versus 2.4% of the moderately ill. This shows that there are these cases where delirium and stroke are common in this population and should be on people's radar. Interestingly, when I was looking at this article, where they were comparing the severe versus the non-threaty. severe COVID-19 patients. Dizziness and headache were about the same between the two groups. Impaired consciousness was much higher in the severe disease COVID-19 patients. And acute cerebrovascular disease was much higher as well in this severe COVID-19 group.

So on April 3rd, 2020, that was yesterday. There was a case report that was published. of acute necrotizing encephalopathy. This was a middle-aged patient who tested negative for other things that might cause it, such as herpes, simplex virus 1 and 2, varicella zoester virus, West Nile virus, and they were also PCR-confirmed diagnosis of COVID-19.

They found an imaging symmetric hypotentiation of the bilateral medial thalomy and hemorrhagic rim-enhancing lesions of the bilateral thalomite, medial temporal lobes, and subinsular regions. I'll put a link to that on my website, on Psychiatrypodcast.com as well. The image is something you can't miss. So although this is rarely seen, acute necrotizing encephalopathy is a serious complication of influenza and other invasive viral conditions.

And the proposed mechanism for the rapid decline in neurocognition is a for debate, but recent articles in The Lancet suggest that cytokime storm has an important implication. Predictors of the fatality from a recent retrospective multi-center study of 150 confirmed COVID-19 patients in Wuhan, China included elevated ferretin, a mean of 1,297 nanograms per ML, and non-survivors versus 614 nanograms per ML, survivors and IL-6 also much higher suggesting that mortality might be due to virally driven hyper inflammation. Still others continue to argue that the spread of the coronavirus through synapse connected routes of the olifactory and lower respiratory areas to the medullary respiratory centers of the brain stem. And so, you know, it's possible that the most important

takeaway from this is that there may be neurological findings with COVID-19 that aren't just stroke and delirium, but also there could be acute necrotizing and cephalopathy. So I wanted to talk a little bit about delirium as well because in studies, you know, it was around 15% of people presenting with severe COVID-19. This is something that we get consulted on for C&L psychiatry. There's both the acute illness, right, which could cause the delirium and the neuroinvasive potential, which could also increase the likelihood of delirium. Older people are at greatest risk for COVID-19.

and if the infection is present and more severe, they are more likely to have delirium. Around 15% will have delirium, although this is not something that can be just seen in older people. So I was thinking about this and I was thinking about how QTC, so QTC is something that we monitor on an EKG to see how much of a risk someone is, going to have for Torsods, which is an arrhythmia.

And if someone has heart failure or heart damage, they're at higher risk for QTC to be an issue. And further, we are giving medications with elevated QTC potential in these patients, Zythromycin and Plaquino. This becomes a problem when all antipsychotics, which is the usual treatment to calm someone down, in the midst of delirium, all antipsychotics except for Abilify increased QTC. So as a CNL psychiatrist, this is something we will be evaluating and considering and weighing

and measuring and monitoring. Patients with COVID-19 have higher risk for cardiovascular disease. There was one physician who was quoted Dr. Bazini, who said there's a dramatic increase in the number of vascular events, ischemic strokes, and thrombosis, which is likely due to the virus affecting the quagulating mechanisms. Stoke patients who are not too compromised for respiratory insufficiency are being treated with tissue plasminogen, activator, and mechanical thrombonectomy, and other means I will leave that to my neurology colleagues to give nuance to. They're also, is a comorbidity of COVID-19 and diabetes and hypertension.

In one study, 48% of patients had comorbidities with hypertension being the most common and with diabetes and cardiac disease being the second and third most common. Just to give you an idea, because this is not only hitting those patients, hypertension was in 30%, diabetes, in 19% of patients and coronary heart disease, comorbidity. So these are things that they had before COVID-19 was in 8% of patients. So in this population, the things that might increase delirium are stroke, the viral

encephalitis, or more severe disease. We know that ICUs in general are related to higher incidence of delirium. And this can be an especially difficult issue in this population because if someone becomes agitated in a delirium, they may pull out lines, they may put staff at risk for infection. And actually, another recent study has showed that the staff were at higher risk if they were working night shifts, if they were working more hours, they were at higher risk for infection. So a little note on the treatment of delirium. Haldol has been shown to be effective for treating delirium in the critical care setting. Ivy Haldol has a known increase in the QTC, which can increase risk of arrhythmia and sudden cardiac death. This needs to be taken into consideration with people with pre-existing cardiac history or acute cardiac injury due to COVID-19.

I was reading in a sort of consensus guidelines that they were talking about doing some test doses of maybe two milligrams of IV in the first 24 hours. Normally, you know, maybe 2 milligrams IV, Q4 is a normal dose. 5 milligrams IMQ6 hours. The IV is more potent than the IM version. And with a howl-all, there is that risk for QTC, so we're monitoring that, and we are considering if that's the best option. Other treatment of delirium is valproc acid, depacode, depacone, depaquin. If you remember from my earlier episode on viparic acid, that at a blood level of 80, you know, blood levels are taken 12 hours after the medication is given,

at a blood level of 80, there will be 10% of the valpric acid free. At a blood level of 120, 30% will be free because of how it binds albumin. So that's something to consider if we are treating these patients and we need to get them up to a level where they're calm and not agitated. Valproc acid has been shown to be efficacious in treating delirium. although we might also note that if the patient has underlying liver compromise, this will not be a good option. Viparic acid has a well-known side effect of hepatic injury and even fatal hepatic toxicity. Patients with COVID-19 have been noted to have higher rates of liver dysfunction and elevated liver transaminases.

So we want to monitor the BUN and LFTs, and which can be elevated in COVID-19 and other inflammatory conditions like septiminases. Another medication, olanzapine, has been shown to be effective in treating delirium. It's another antipsychotic. It also prolongs QTC. In one study in 2015, they showed that halidol, haloperidol, rsperidone, olanzapine, and apriiprizo had comparable efficacy. That being said, I would be less likely to use an antipsotic like suprasidone because it has a lot more QTC prolongation, I would be more likely to use eriprizole, which has been shown to be

as effective as Haldol in one study of 30 to 15 milligrams per day. The agitation, disorientation, confusion improved from a mini mental status of five to 28. That was pretty significant over the course of those days. And this might be a good option, except if they're on a ventilator and not taking anything PO, that'll make it more difficult. And that's when how they might be the option of choice. So, airperazole has minimal effects on QTC, which makes it one of my more favorites for treating delirium. There's other medications as well. Dex metatomodine, Presidex, is another option.

It's an alpha-2 agonist, which is sometimes used for sedation, analgesic effects in post-operative delirium in an ICU setting. It has minimal respiratory depression, which is useful considering the respiratory complications of COVID-19, but can cause bradycardi and hypotension due to its sympathetic and vagalimetic effects. So this is something to consider, but realize that if they're also having cardiac complications, it might not be the best fit.

Usually the dose is around 0.2 micrograms per kilogram per hour, and the elderly with a maintenance dose of around 0.7 micrograms per kilogram per hour, doses above 1.5 micrograms per kilogram per hour have not been shown to have increased clinical efficacy. There have been some recent studies that have talked about melatonin. Melatonin is currently being investigated as an adjunctant of treatment due to its anti-inflammatory and anti-oxidative effects that have been well studied in Ard's acute respiratory distress syndrome, which COVID-19 is commonly associated with. So melatonin might be something that is used more commonly.

There's one recent paper, and here's two quotes from it. It's a tan 2020. Here's the quote, melatonin is a molecule that displays respective properties since it downregulates the overreaction of the innate immune response and overshooting inflammation, but also promotes the adaptive immune activity. If melatonin was given at one milligram per kilogram subcontaneously for three days before and 10 consecutive days after inoculation, the mortality of the infected mice was reduced from 100% in untreated animals to 16%. Moreover, the high tighter of IGM antibodies were found from three to seven weeks after virus inoculation.

The dose of one milligram per kilogram is for a 70% percent. kilogram body weight human subject easily achievable and has no or only small side effects for several months of use in humans. This seems like something that should be looked at and really considered because it is low side effect. These are much bigger doses than we give for sleep. Usually we only go up to 10 milligrams for sleep. I would be taking basically 100 milligrams of this. per day with my body weight, maybe a little bit more. Okay, so talking a little bit about the treatments that are currently being used for COVID-19 from a psychiatrist's perspective of all these other meds that we're given as well,

the chloroquine, hydroxychloroquine has been shown to inhibit the COVID-19 replication and elimination of the COVID-19 virus from the body. However, studies have shown that that chloroquine prolongs QTC. So this should be something that's taken into account when we are giving other medications that prolong QTC. Zythromycin has also been shown to be an effective adjunct to hydroxy chloroquine in reducing viral load in COVID-19 patients. Asythromycin, as well as other macrolides have been known to increase QTC, which can. increase risk of cardiac arrhythmias, torsades to points. The risk is increased in elderly women with coexisting heart disease that were taking QTC prolonging drugs. So extra care

needs to be taken with this population as they are at higher risk for delirium and poor outcomes associated with COVID-19. There's an antiviral called REM desivir. It's a broad spectrum antiviral, which has been found to block viral replication in SARS and MERS and has been found to block SARS-Cove-2 infection in vitro. There is no current research being done that looked at the drug-drug interactions that we could find with the other medications. So take that into consideration. Also high-dose IV vitamin C is currently being investigated as an adjective of treatment. It has been found to reduce mortality rates in patients with sepsis and ards, both of which commonly associated patients in the ICU on ventilator support and now severe

COVID-19 infections. So that's another proposed treatment for COVID-19. A word on insides. We know the tweet that came out from France saying don't use insides. They're commonly used in general for people with sore throat, fever, but newer studies have shown that maybe it prolongs illness by depressing the immune response and results in more severe illness and complications. And I'll put this article because I don't know if I would have believed it if I wouldn't have read these articles.

This correlates with other research that Ensod's use in community acquired pneumonia was associated with pluripulmonary complications and more complicated recovery course. So I would recommend Tylenol, acetaminophen, instead of ibuprofen. Corticosteroids have previously been used for SARS and MERS, however, corticosteroids in treating COVID-19

is not currently recommending as there has not been shown to be any benefit and maybe more harm than good. It shows the risk of corticosteroids may increase mortality, increased secondary infections, impaired clearance of the SARS-cove 2 and prolonged viral shedding, and other side effects of corticosteroid therapy such as psychosis and delirium.

So initially when I was thinking about what medications might be, be used to treat COVID-19. I was thinking corticosteroids, but I think actually after reading these papers, it's probably not a good treatment. And, you know, I was thinking it might be used to treat it and all the psychiatric manifestations of things that can come from steroids. But it turns out that it's probably not something that they're going to be using. That might be different, by the way, for people who have the encephalitis.

the viral encephalitis, specifically what I talked about before with the acute necrotizing encephalopathy, it looks like they treated with some corticosteroids. So sometimes that's used to decrease swelling in the brain. So there's a lot of nuance in both the treatments and the side effects of the treatments. I think it's worth talking a little bit about antibodies. to the coronavirus. So there's both convalescent plasma. So this is people who were infected with the coronavirus. And so the plasma distills the antibodies that they have in their blood still to the coronavirus.

And then basically you can give this to patients who are sick. I think that's a wonderful treatment. And that's a good option. The second thing is producing coronavirus antibodies in a lab. This is done by isolating B cells from people who have had coronavirus, making them produce a ton of antibodies, purifying them, and then administering them to patients. This is what they did for Ebola, and I think it's promising.

Another option is testing antibody treatments already on the market for other conditions, with potential crossover benefits for COVID-19 patients. Further, another option is a coronavirus fighting antibodies from mice. So you try to make these antibodies as human-like as possible. There have been questions of can you take antibody treatments before you get sick to prevent illness? And this was used for kids, actually, for RSV. Because there's no RSV vaccine, they would give lab-grown antibodies to high-risk children. So I wonder if we should be giving these to people on the front lines of treatment, or sorry, the front lines medical workers, if we should be giving them antibodies

so that if they do get infected, they would have lower risk for disease. Further, all of this pointing towards the strong importance of PPE to protect our health care workers. It's a, It's a true tragedy that we were not prepared for this and that there's been such a shortage. So other thoughts on the treatment of things like delirium, it's possible we should do early screening. We should reduce the risk of healthcare workers getting the disease from patients who are potentially delirious. I think that mechanical restraints are indicated at times when otherwise there are not effective treatments or treatments would cause other side effects that would put the patient at risk of death. So we should try to reduce the risk of delirium in these patients by reducing precipitating factors, optimizing medical illnesses, not letting patients get too dehydrated or malnourished. cognitive impairment, optimizing cognitive impairment.

Can we optimize vision and hearing impairment? Using physical restraints, having patients not go into urinary retention or convent, preventing constipation and preventing pain in polypharmacy. So there's things that we can do to reduce the risk of delirium. And if we can do that, it's the best treatment. obviously if you get it beforehand. I know in our department, we are trying to move to do telepsychiatry for these delirious patients. I've read on forums that talking to the nursing staff, getting a history from the physician,

and maybe not even going into the room, but just treating the patient presumptively if they have delirium and it's obvious, it might be more prudent to not go in and do a physical exam. And physical exam is pretty limited usually in these patient populations. So if it's pretty clear cut, maybe just doing more of a sidewalk consult would be more prudent to reduce risk of transmission and reduce risk to the healthcare workers themselves. But at our institution, we are moving towards doing more of a telepsychiatry consult service to reduce the risk to our staff. So in conclusion, this has been a little bit more of a sober talk thinking through like what this, you know, what are some treatment modalities, what are some potential obstacles we're going to have as a psychiatric force treating this disease. It is, it is a sobering time. It's a war time of sorts in the medical, in the medical world.

And you feel it. You feel it on, you know, the internal medicine doctors. the people are on the front lines treating this disease. And, you know, as a psychiatrist, being in the trenches, hearing the anxiety all day, it does something to you. And you have to stay grounded. You have to practice self-care. I've been going for more walks.

I've been eating healthy, trying to, you know, fast a little bit in the morning, do some intermittent fasting, doing some swimming, playing with the kids a lot when I am home. and I hope that you are practicing some self-care as well. And I know if you're a physician or if you're a nurse listening to this, if you're on the front lines treating these patients and you feel exhausted, of course you're entitled to you. I mean, you know, there are psychiatrists who are and therapists

who would love to connect with you if you are struggling. This is a time that we all can rally together. and we can make the best of a very difficult situation. You know, I think in large part we were in a sort of, you know, we were like indoor cats and now we're like outdoor cats. The average life expectancy of indoor cats is about three times as long as outdoor cats. And sometimes with all of the many benefits that come with being a post-industrialized society, and we're just used to a level of security and we're in insecure times.

We're in times where it's a little bit more of sobering. And I feel it. I feel the intensity of it. I feel the intensity of this time. I feel in these times of, you know, kind of like a wake-up call to the realities of life, the potential of death. It can be good to see people rally together. And I have seen my department closer than ever.

And we are having daily updates, daily phone calls, Zoom calls, talking about what's going on, talking about how to manage the inpatient psychiatric units in these times, talking about how to manage the CNL services in these times. And secondly, you know, I'm well aware. that today is April 4th and that in one week there may be, you know, updates to this that are needed. And so, you know, I am operating on the best information that I can at the time of recording this. And I'm sure that new things will be found.

Things will be disproved that we thought to be the case. and new treatments will be found that are exciting. I personally am concerned of the viral illness itself, but then also the psychological manifestations of everything that's coming with us, such as the unemployment, increased tension in marriages, increased stress on our economy, on our psychological and physical health. And I'll be talking about this in coming weeks, talking about things that we can do to cope with this.

So this episode is more for the healthcare workers who are in the trenches, who are making these, who are going to be evaluating and treating these patients. And I hope this has been helpful for you. There will be this blog with all the citations. There's probably about maybe 100 citations on this one. And it will be on my website, Psychiatrypodcast.com. It will also be in my resource library linked in the show notes. I want to thank all of my, the supporters of this podcast.

It's been really meaningful to hear your messages. A lot of you have written me personal messages when you sign into the resource library, and I read those, and I really appreciate them. So I wish you guys a good day. I hope you are well. I hope you're physically well and psychologically well. I hope that if you're not yet infected with this, you know, focus on your own health, getting good sleep, exercising. It's a good time to quit smoking.

It's good time to spend time with family and friends. There's some stoic philosophy that really fits this time well that says, you know, without fear to looking at the end of your life and consider living each day as if it is your life. day or each conversation. And I went into this talk with that thought of how do I share some things that might help in the midst of this time. If I can equip the medical professionals out there just a little bit more, it'll be meaningful. So, all right, we'll leave it there.